As a practical strategy for reducing agitation in schizophrenia, low-potency neuroleptics have been commonly used as an adjunct in combination with high-potency neuroleptics that seem superior in reducing positive symptoms. There is no evidence, however, that giving more than one antipsychotics at a time enhances therapeutic effects. Antipsychotic polypharmacy has been rather considered an unproven and potentially harmful practice [4].

The low-potency neuroleptic levomepromazine has been in common use for agitated patients with schizophrenia in Europe and Japan [2,3], because of its markedly sedative property. In order to clarify whether levomepromazine as an adjunct to high-potency neuroleptics are beneficial or harmful, therefore, we compared the efficacy of the combined therapy with levomepromazine and high-potency neuroleptic haloperidol with the monotherapy with haloperidol for patients with acute exacerbation of schizophrenia.

We have followed up a patient with 8q24.2 → qter and 15q14 → pter duplication due to a maternal reciprocal translocation, a condition related to Prader-Willi Syndrome. Apart from dysmorphic features, the patient suffered from recurring episodes of bipolar psychosis. Interestingly, PET scanning revealed revealed prominent bilateral hypometabolism in the frontal, temporal, and parietal lobes as well as in the cerebellum. Possible implications of this rare chromosomal abnormality with regards to psychiatric disorders are discussed, with emphasis on recent evidence suggesting chromosome 15q13-15 as a susceptiblity locus for psychosis.

Sir: Studies concerning depression in primary care emphasize the fact that several clinical features of these mood disorders do not satisfy the diagnostic criteria of psychiatric classifications [4]. These primary care patients have been classified as subclinical depression, subthreshold depression, or patients with “depressive symptoms only” [2]. We compared using analysis of variance and Mann–Whitney statistics, a randomized group of 43 patients presenting clinical depressive symptoms (Beck Depression Inventory >16, cut-score validated in Spanish version [1,3]), with another group of 41 “subclinical” patients (BDI scores: 10–16). We considered statistically significative difference P < 0.01.

Fifty clinically stable, schizophrenic outpatients, suffering from residual schizophrenic symptoms and/or neurological side effects, were randomised to either continue their conventional neuroleptic(s) or change it to olanzapine. After 12 weeks patients on olanzapine exhibited significant improvement in neurological side effects and psychotic symptomatology as compared to patients on conventional antipsychotics.

In a double blind controlled study, rTMS results in a similar antidepressant effect to sham in combination with paroxetine. Both groups had the same delay in scale’s scores improvement. rTMS seems not to be efficient as an add-on treatment to pharmacological medication in non-resistant major depression.

The treatment of depressive symptoms in patients affected by schizophrenia is often a concern for clinicians [2] due to potential interaction, in terms of safety and efficacy. Citalopram seems to be a safe SSRI as adjunctive treatment to Olanzapine because of the lack of interactions. We report a serendipitous finding showing that the adjunction of Citalopram to Olanzapine, led to disappearence of residual hallucinations and depersonalization symptoms in a few weeks.

Mr A is a 27-year-old male, living in the community, with a 4-year history of schizophrenia,. He was treated with low doses of Olanzapine (10 mg/daily) since 2000 because of an intolerance to dose increments (weight gain and mydriasis).The persistence of sporadic hallucinations (commenting voices) and depersonalization symptoms (when he walked alone he felt his self leaving the body) was well tolerated by the patient. The social functioning was satisfactory: he had a protected job and was involved in a comprehensive rehabilitation programme.